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        Growth of Intermetallic Phases in Al/Cu Composites at Various Annealing Temperatures During the ARB Process

        Chih-Chun Hsieh,Ming-Shou Shi,Weite Wu 대한금속·재료학회 2012 METALS AND MATERIALS International Vol.18 No.1

        The purpose of this study is to discuss the effect of annealing temperatures on growth of intermetallic phases in Al/Cu composites during the accumulative roll bonding (ARB) process. Pure Al (AA1100) and pure Cu (C11000) were stacked into layered structures at 8 cycles as annealed at 300 °C and 400 °C using the ARB technique. Microstructural results indicate that the necking of layered structures occur after 300 °C annealing. Intermetallic phases grow and form a smashed morphology of Al and Cu when annealed at 400 °C. From the XRD and EDS analysis results, the intermetallic phases of Al2Cu (θ) and Al4Cu9 (γ2) formed over 6 cycles and the AlCu (η2) precipitated at 8 cycles after 300 °C annealing. Three phases (Al2Cu (θ), Al4Cu9 (γ2), and AlCu (η2)) were formed over 2 cycles after 400 °C annealing.

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        Toxoplasma gondii induces autophagy and apoptosis in human umbilical cord mesenchymal stem cells via downregulation of Mcl−1

        Chu, Jia-Qi,Jing, Kai-Peng,Gao, Xiang,Li, Peng,Huang, Rui,Niu, Yan-Ru,Yan, Shou-Quan,Kong, Jun-Chao,Yu, Cai-Yuan,Shi, Ge,Fan, Yi-Ming,Lee, Young-Ha,Zhou, Yu,Quan, Juan-Hua Landes Bioscience 2017 Cell Cycle Vol.16 No.5

        <P>Autophagy and apoptosis are critical for controlling Toxoplasma gondii (T. gondii) infection. T. gondii infection during pregnancy can damage the fetus and cause birth defects; however, the molecular mechanisms of this process are poorly understood. This study aims to determine the activities of autophagy and apoptosis as well as their regulatory mechanisms during T. gondii infection by using human umbilical cord mesenchymal stem cells (hUC-MSCs) as a model of congenital diseases. LC3B, a hallmark protein of autophagy was incrementally upregulated with the infection duration, whereas p62 was downregulated in T. gondii-infected hUC-MSCs. Concurrent to this result, the invasion of T. gondii into hUC-MSCs increased in a time-dependent manner. The expression levels of Bcl-2 family proteins including Bcl-2, Bcl-xL, Bim, Bax, Bid and Bak were not altered; however, Mcl-1 levels in hUC-MSCs were dramatically decreased upon T. gondii infection. In addition, at 24h post-infection, cleaved PARP and cleaved caspase-3 protein levels were elevated in hUC-MSCs. Importantly, Mcl-1 overexpression reduced the levels of autophagy- and apoptosis-related proteins in T. gondii-infected hUC-MSCs. Mcl-1 proteins were primarily expressed in the fraction containing mitochondria and strongly interacted with Beclin-1 under normal conditions; however, these interactions were remarkably attenuated by T. gondii infection. These results suggest that mitochondrial Mcl-1 is an essential signaling mediator regulating the activation of autophagy and apoptosis during T. gondii infection.</P>

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